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Department of
Pneumology, Hotel-Dieu, 75181 Paris Cedex 04, France
Correspondence to: Professor J-P Laaban j-pierre.laaban{at}htd.ap-hop-paris.fr
Received 19 April 1999; Returned to authors 9 July 1999; Revised version received 24 March 2000; Accepted for publication 25 July 2000
BACKGROUND
Pulmonary
arterial hypertension (PAH) in patients with sleep apnoea syndrome
(SAS) is classically ascribed to associated chronic obstructive
pulmonary disease (COPD). The aim of this retrospective study was to
evaluate the possible occurrence of PAH as a complication of SAS in
patients without COPD.
METHODSRight heart
catheterisation was performed in 44 patients with SAS and without COPD
confirmed by polysomnography (apnoea index >5/h) admitted for the
administration of nasal continuous positive airway pressure (CPAP).
RESULTSPrecapillary
PAH, defined as mean pulmonary arterial pressure of >20 mm Hg with
pulmonary capillary wedge pressure <15 mm Hg, was observed in 12/44
(27%) patients with SAS. There were no significant differences in
apnoea index between patients with (PAH+) and those without PAH (PAH-)
(42.6 (26.3) versus 35.8 (21.7) apnoeas/h). The PAH+ group differed
significantly from the PAH- group in the following respects: lower
daytime arterial oxygen tension (PaO2) (9.6 (1.1) versus 11.3 (1.5) kPa, p=0.0006); higher daytime arterial carbon
dioxide tension (PaCO2) (5.8 (0.5) versus 5.3 (0.5) kPa, p=0.002); more severe nocturnal hypoxaemia with a higher
percentage of total sleep time spent at SaO2
<80% (32.2 (28.5)% versus 10.7 (18.8)%, p=0.005); and higher body
mass index (BMI) (37.4 (6) versus 30.3 (6.7) kg/m2,
p=0.002). The PAH+ patients had significantly lower values of vital
capacity (VC) (87 (14)% predicted versus 105 (20)% predicted, p=0.005), forced expiratory volume in one second (FEV1) (82 (14)% predicted versus 101 (17)% predicted, p=0.001), expiratory
reserve volume (40 (16)% predicted versus 77 (41)% predicted,
p=0.003), and total lung capacity (87 (13)% predicted versus 98 (18)%
predicted, p=0.04). Stepwise multiple regression analysis showed that
mean pulmonary artery pressure (PAPm) was positively correlated with BMI and negatively with PaO2.
CONCLUSIONPulmonary
arterial hypertension is frequently observed in patients with SAS, even
when COPD is absent, and appears to be related to the severity of
obesity and its respiratory mechanical consequences.
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